摘要
目的 探讨bcl 2与FAS在NO介导的重型肝炎肝细胞凋亡中的作用。方法 雌性Balb/C小鼠 2 4只随机分为A、B、C、D 4组 ,每组 6只 ,分别为正常对照组、模型组、L Arg干预组 (NO供体干预 )、L NAME干预组 (NOS抑制剂干预 )。各组动物均于用药后 6h处死 ,留取血清、肝组织。用Griess法测定血清NO代谢产物NO-2 ,TUNEL原位检测肝细胞凋亡状况并计算凋亡指数 ,免疫组织化学法检测各组肝组织Fas表达及原位杂交技术检测各组肝组织bcl 2mRNA的表达。结果 1.应用NO合成干预因素后 ,C组及D组NO-2 水平分别较B组升高及降低。 2 .正常肝组织经TUNEL检测未见凋亡细胞 ,其凋亡指数为 0。B组存在肝细胞凋亡现象 ,凋亡指数为 16 2 7% ,C组凋亡指数上升 (2 4 5 2 % ) ,而D组凋亡指数下降 (7 92 ) % ,组间比较有显著性差异 ,P值 <0 0 1。 3.正常肝细胞内未见Fas蛋白及bcl 2mRNA表达。B组Fas表达较广泛 ,C及D组Fas表达呈不同程度的增强和减弱 ;组间比较差异有显著性 ,P值 <0 0 1。B组及C组均未见bcl 2mRNA杂交信号 ,仅D组见肝细胞内出现杂交信号。结论 高水平的NO具有明显的促进肝细胞凋亡的作用。NO对于肝细胞的损伤可以通过介导凋亡的方式实现。NO在介导肝细胞凋亡的过程中 ,启动了FAS凋亡途径 ,而抑制NO的过量产生可?
? Objective To study the role of bcl-2 and FAS in NO-mediated hepatocyte apoptosis during hepatitis gravis. Method Female Balb/C mice were divided randomly into four groups: A (normal control), B (model group), C (NO donor group) and D (NO inhibitor group). The production ofNO in the serum was assayed with Griess method, the hepatocyte apoptosis was estimated by TUNEL methods, and the expression of FAS and bcl-2mRNA in liver cells was observed by immunohistochemistery and in situ hybridyzition. Result Compared with group B, the level of serum NO- 2was increased in group C but reduced in group D. The apoptotic cells could not be found in normal liver tissues. The apototic index was 16.27% in gruop B, increased to 24.52% in group C, but decreased to 7.92% in group D; and the differences between these groups were significant.There was no expression of FAS protein and bcl-2 mRNA in normal liver tissues. The expression of FAS was extensive in group B, reinforced in group C but weakened in group D. There was no hybridyzation signal of bcl-2 mRNA in the hepatocytes of group A, B and C, except group D. Conclusion The results show thathigh leverof NOcan induce hepatocyte apoptosis and this may be involved in upregulating Fas and downregulating bcl-2. 〔
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2002年第4期434-438,513,共6页
Chinese Journal of Histochemistry and Cytochemistry
基金
国家自然科学基金资助(No.39270314)
